Evidence map›Paper›PMID 41378489›Full record

ArticleJournal of the American Heart Association2025

Changes in Expression Profiles of Caspase-8 and Mixed Lineage Kinase Domain-Like Protein/Receptor-Interacting Protein Kinase 3 Mediated by Inflammation in Cerebral Arteriovenous Malformations Associated With Clinical Condition on Admission.

Kenji Shimada, Izumi Yamaguchi, Takeshi Miyamoto, Masaaki Korai, Hiroshi Koyama, Noriya Enomoto, Alfredo Shimabuku, Keiko T Kitazato, Yasuhisa Kanematsu, Yasushi Takagi

Abstract read
In one paragraph

Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Kenji ShimadaDepartment of Neurosurgery Tokushima University Tokushima Tokushima Japan.ORCID 0000-0002-2262-9243
Izumi YamaguchiDepartment of Neurosurgery Tokushima University Tokushima Tokushima Japan.ORCID 0000-0001-9005-1570
Takeshi MiyamotoDepartment of Neurosurgery Tokushima University Tokushima Tokushima Japan.ORCID 0000-0001-9136-1829
Masaaki KoraiDepartment of Neurosurgery Tokushima University Tokushima Tokushima Japan.ORCID 0000-0002-5326-3467
Hiroshi KoyamaDepartment of Neurosurgery Tokushima University Tokushima Tokushima Japan.
Noriya EnomotoDepartment of Neurosurgery Tokushima University Tokushima Tokushima Japan.
Alfredo ShimabukuDepartment of Neurosurgery Tokushima University Tokushima Tokushima Japan.ORCID 0000-0002-4902-6717
Keiko T KitazatoDepartment of Neurosurgery Tokushima University Tokushima Tokushima Japan.
Yasuhisa KanematsuDepartment of Neurosurgery Tokushima University Tokushima Tokushima Japan.
Yasushi TakagiDepartment of Neurosurgery Tokushima University Tokushima Tokushima Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCerebral arteriovenous malformations (cAVMs) are complex vascular anomalies carrying a high risk of hemorrhage due to abnormal arteriovenous connections. Recent studies have highlighted the roles of inflammation and

methodsWe analyzed tissue samples from 23 patients with cAVM in comparison with normal brain tissues. Proteome profiling, immunohistochemistry, and quantitative polymerase chain reaction assays were used to assess the expression of inflammatory molecules and programmed cell death markers.

resultsProtein and gene expression of necroptosis-related molecules (RIPK3, MLKL), caspase-8, and IL-6 (interleukin-6) and IL-8 were significantly elevated in cAVM nidi compared with normal brain tissue. High MLKL protein expression was associated with severe clinical presentations and hemorrhage, whereas caspase-8 protein expression was elevated in less-severe cases and unruptured cAVM.

conclusionOur analysis of human samples offers the first evidence of necroptosis-related molecules acting against caspase-8 in association with the inflammatory cytokines IL-6 and IL-8 in the pathogenesis of cAVM. The balance between MLKL and caspase-8 expression may be linked to the clinical condition and hemorrhagic presentation of patients with cAVM on admission.

Indexed as

Caspase 8InflammationIntracranial Arteriovenous MalformationsProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesAdolescentAdultCerebral HemorrhageFemaleHumansInterleukin-6Interleukin-8MaleMiddle AgedNecroptosisYoung AdultCASP8 protein, humanCaspase 8CXCL8 protein, humanIL6 protein, humanInterleukin-6Interleukin-8MLKL protein, humanProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humancaspase‐8cerebral arteriovenous malformationinterleukin‐6interleukin‐8necroptosis

Identifiers

PMID41378489
PMCPMC12826922

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.